The effect of saraglitazar on TGF-β-induced smad3 phosphorylation and expression of genes related to liver fibrosis in LX2 cell line.

Background And Purpose: Liver fibrosis is a reversible liver injury that occurs as a result of many chronic inflammatory diseases and can lead to cirrhosis, which is irreversible and fatal. So, we studied the anti-fibrotic effects of saroglitazar on LX-2 cell lines, as a dual PPARα/γ agonist.

Methods: Cells, after 80% confluence, were treated with TGF-β (2 ng/mL) for 24 h.

Curcumin Modulates NOX Gene Expression and ROS Production via P-Smad3C in TGF-β-Activated Hepatic Stellate Cells.

Background: Liver fibrosis, associated with hepatic stellate cells (HSCs), occurs when a healthy liver sustains damage, thereby impairing its function. NADPH oxidases (NOXs), specifically isoforms 1, 2, and 4, play a role in reactive oxygen species (ROS) production during hepatic injuries, resulting in fibrosis. Curcumin has shown strong potential in mitigating liver fibrosis.

Comparison of the anti-inflammatory and antilipidemic activity of diosmin and saroglitazar in a model of nonalcoholic fatty liver induced by a high-fat diet in Wistar rats.

Objectives: Non-alcoholic fatty liver disease (NAFLD) is the most common liver-related metabolic disorder in the world, with a global prevalence of 25%. Compounds with anti-inflammatory, lipid-lowering, and insulin-sensitizing properties can be used for the prevention or treatment of NAFLD. Therefore, this study was conducted to investigate the effect of saroglitazar (a dual PPARα/γ agonist) and diosmin (a flavonoid) on non-alcoholic fatty liver induced by a high-fat diet (HFD) in Wistar rats.

The Effect of Lipopolysaccharide-Stimulated Adipose-Derived Mesenchymal Stem Cells on NAFLD Treatment in High-Fat Diet-Fed Rats.

Background: Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are 2 common liver diseases that currently lack effective treatment options.

Objectives: This study aimed to investigate the effect of lipopolysaccharide (LPS)-stimulated adipose-derived stem cells (ADSCs) on NAFLD treatment in an animal model.

Methods: Male Wistar rats were fed a high-fat diet (HFD) to induce NAFLD for 7 weeks.

Isorhamnetin Exerts Antifibrotic Effects by Attenuating Platelet-Derived Growth Factor-BB-induced HSC-T6 Cells Activation via Suppressing PI3K-AKT Signaling Pathway.

Background: Currently, liver fibrosis is growing worldwide; unfortunately, there is no definite cure for this disease. Hence, understanding the molecular pathways involved in the development of liver fibrosis can help to find a proper treatment. In this study, we aimed to evaluate the effects of isorhamnetin as an antifibrotic agent on platelet-derived growth factor (PDGF)-BB-activated hepatic stellate cells (HSC)-T6 cells in a concentration-dependent manner.

Effects of exosomes of mesenchymal stem cells on cholesterol-induced hepatic fibrogenesis.

Objectives: Free cholesterol in the diet can cause liver fibrosis by accumulating in Hepatic stellate cells (HSCs). The rate of mortality of this disease is high worldwide and there is no definite remedy for it, but might be treated by anti-fibrotic therapies. MSCs-derived exosomes are known as the new mechanism of cell-to-cell communication, showing that exosomes can be used as a new treatment.

Exosomes of Whartons' jelly mesenchymal stem cell reduce the NOX genes in TGF-β-induced hepatic fibrosis.

Objectives: Activated cells which are called star-shaped cells, are some of the key factors in the development of liver fibrosis. Activation of NADPH oxidase (NOX) is associated with increased HSCs activity and progression of hepatic fibrosis. In this study, the effects of human exosomes derived from WJ-MSCs on NOX1, NOX2, and NOX4 gene expression in TGF-β-induced hepatic fibrosis were investigated.

Comparison of the effects of cholesterol, palmitic acid, and glucose on activation of human hepatic stellate cells to induce liver fibrosis.

Background: In hepatic damage, Hepatic stellate cells (HSCs) become active, proliferate, and change to myofibroblasts. Increasing the fibrogenic genes, such as Transforming growth factor-β (TGF-β), Alpha Smooth Muscle Actin (α-SMA), and Collagen1 α (COL 1α) show that the activation of HSCs can lead to hepatic fibrosis.

Purpose: These days people consume much cholesterol, palmitic acid, and glucose which can have adverse effects on an individuals' health, but their influences on activating human HSCs and inducing liver fibrosis have not been assessed.

Effect of Quercetin on the fructose-activated human hepatic stellate cells, LX-2, an in-vitro study.

Background: Hepatic fibrosis is one of the main reasons for mortality in the world. Hepatic stellate cells (HSCs) activate during chronic liver injury, express more Transforming growth factor beta (TGF-β), Collagen1α (COLA1) and actin-alpha smooth muscle (αSMA) that lead to hepatic fibrosis. Quercetin is a flavonoid in vegetables and fruits that has shown hepatoprotective potential, but little is known about its effects on HSCs activation.